<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Todorova K</submitter><funding>Bulgarian National Science Fund</funding><pagination>28-48</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10355945</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><pubmed_abstract>Cancer progression is driven by genome instability incurred rearrangements such as transmembrane protease, serine 2 (TMPRSS2)/v-ets erythroblastosis virus E26 oncogene (ERG) that could possibly turn some of the tumor suppressor micro-RNAs into pro-oncogenic ones. Previously, we found dualistic miR-204 effects, acting either as a tumor suppressor or as an oncomiR in ERG fusion-dependent manner. Here, we provided further evidence for an important role of miR-204 for TMPRSS2/ERG and androgen receptor (AR) signaling modulation and fine tuning that prevents TMPRSS2/ERG overexpression in prostate cancer. Based on proximity-based ligation assay, we designed a novel method for detection of TMPRSS2/ERG protein products. We found that miR-204 is TMPRSS2/ERG oncofusion negative regulator, and this wa</pubmed_abstract><journal>Hormones &amp; cancer</journal><pubmed_title>Micro-RNA-204 Participates in TMPRSS2/ERG Regulation and Androgen Receptor Reprogramming in Prostate Cancer.</pubmed_title><pmcid>PMC10355945</pmcid><funding_grant_id>DMU 03/27</funding_grant_id><pubmed_authors>Fernandez N</pubmed_authors><pubmed_authors>Mincheff M</pubmed_authors><pubmed_authors>Todorova K</pubmed_authors><pubmed_authors>Metodieva G</pubmed_authors><pubmed_authors>Metodiev MV</pubmed_authors><pubmed_authors>Hayrabedyan S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Micro-RNA-204 Participates in TMPRSS2/ERG Regulation and Androgen Receptor Reprogramming in Prostate Cancer.</name><description>Cancer progression is driven by genome instability incurred rearrangements such as transmembrane protease, serine 2 (TMPRSS2)/v-ets erythroblastosis virus E26 oncogene (ERG) that could possibly turn some of the tumor suppressor micro-RNAs into pro-oncogenic ones. Previously, we found dualistic miR-204 effects, acting either as a tumor suppressor or as an oncomiR in ERG fusion-dependent manner. Here, we provided further evidence for an important role of miR-204 for TMPRSS2/ERG and androgen receptor (AR) signaling modulation and fine tuning that prevents TMPRSS2/ERG overexpression in prostate cancer. Based on proximity-based ligation assay, we designed a novel method for detection of TMPRSS2/ERG protein products. We found that miR-204 is TMPRSS2/ERG oncofusion negative regulator, and this wa</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Feb</publication><modification>2026-05-28T09:01:30.528Z</modification><creation>2025-02-19T04:25:18.919Z</creation></dates><accession>S-EPMC10355945</accession><cross_references><pubmed>28050800</pubmed><doi>10.1007/s12672-016-0279-9</doi></cross_references></HashMap>